Research is being conducted on the biological mechanisms which control proliferation of various cell types in diabetic retinopathy which include fibroblasts, glia, pigment epithelium, and vascular smooth muscle. Using wound repair as a general model, we have demonstrated that glial cells exhibit chemotaxis to platlet-derived growth factor (PDGF) in a fashion similar to that described in previous reports on smooth muscle and fibroblasts. Pigmented epithelial cells are currently being evaluated for chemotaxis to PDGF. As a consequence of the general wound repair model, each of these cell types is, in turn, being evaluated as a possible source of soluble factors which may be involved in neovascularization.